As our previous studies suggested that some cases of human aplastic anemia may be secondary to persistant viral infections, the study of virus-induced bone marrow suppression may give insights into the etiology and patho- genesis of this human disease. Feline leukemia virus (FeLV), a slowly transforming retrovirus, is the most common cause of erythroid hypoplasia and aplastic anemia in domestic animals. In vitro exeriments have shown that certain strains can selectively inhibit the proliferation of the more mature erythroid progenitor (CFU-E), while the proliferation of the more primitive erythroid progenitor (BFU-E) and the myeloid progenitor (CFU-C) is unaffected. This effect may be related to the higher cycling rate of CFU-E. Feline panleukopenia virus (FPV), a feline parvovirus which usually causes leukopenia in vivo, has been shown to inhibit the proliferation of both myeloid and erythroid progenitor cells in both short- and long-term bone marrow cultures. In addition, a better system for titering FPV has been devised. Previous work has elucidated the pathophysiology of a human parvovirus that is responsible for transient aplastic crises in children with chronic hemolytic anemias. In an attempt to better analyze specimens for the presence of this virus, "Western" blotting and DNA "dot" blotting methods have been devised. Using cloned parvovirus as a probe, attempts have been made to detect intergrated parvovirus DNA in the genome of patients with aplastic anemia. As the etiolgy of most cases of human aplastic anemia is unknown, bone marrow and peripheral blood cultures from these patients were started in an attempt to recover a pathogenic virus. As the culture supernatants from some patients have low levels of reverse transcriptase activity, an enzyme felt to be unique to retroviruses, this suggests that some cases of human aplastic anemia may also be associated with a retroviral infection.